There has emerged in recent years great interest in mercury vapor toxicity and considerable speculation about the danger it represents to selected groups of individuals whose occupations require that they work in a confined environment where metallic vapor is present. To date, relatively little information is available on the early biochemical or behavioral changes resulting from mercury exposure, even though there is a general consensus that the central nervous system (CNS) is altered in the early phase of exposure. Ethanol has been shown in our laboratory to amplify the early and perhaps subtle actions of mercury. Preliminary studies showed that the alcohol sleep-time of mercury-vapor exposed mice was prolongaed. We therefore propose to study the early effects of low level mercury exposure on the CNS by the use of the CNS active drug, alcohol. In addition, this approach will yield valuable information on the possible interactions of mercury with this widely used and often abused drug. Mice will be subjected to mercury vapor exposure at different concentrations and intervals. Alcohol sleep-time of the mice will be determined before and after mercury exposure. The critical concentration of mercury and duration of exposure which will prolong alcohol sleep-time can thus be assessed. Dose-relationship in the development of subclinical toxicity from mercury vapor as detected by alcohol sleep-time will be established. Finally, distribution of mercury in the brain will be examined. Correlation between changed alcohol sleep-time and regional mercury level in the brain will be sought. Finally, the latter will also be correlated to regional catalase activity since this enzyme is believed to be responsible for the oxidation of elemental mercury to charged mercury at least in the red blood cell system.